Strokes Flashcards
1
Q
Ischemic Stroke
Definition
A
The sudden death of brain cells in a localized area due to inadequate blood flow.
2
Q
Stroke
Diagnosis
A
- Pathological dx defined by irreversible ischemic damage to the brain ⇒ cerebral infarction
- MRI immediately positive on DWI (93% of the time)
- ⊕ on CT within 24-48 hours
- ⊖ MRI/CT does not r/o stroke ⇒ if strong suspicion of infarct based on clinical findings can dx stroke
3
Q
Stroke
Epidemiology
A
- #2 killer in the world, #3 in USA
- #1 disabling illness worldwide
- Stroke kills almost 130k Americans each year
- Every year, > 795k people in the US have a stroke
- Recovery is fraught with complications such as aspiration pneumonias and a variety of other infections, DVT and clinical depression
- Rehab while helpful rarely restores a person to his prior functioning and even less often the ability to return to work
4
Q
Stroke Subtypes
A
-
Large vessel thrombotic:
- Thromboocclusive
- Thromboembolic
- Small vessel thrombotic ⇒ Lacunar
- Cardioembolic
- Watershed
- Venous thrombosis
- Transient ischemic attack (TIA)
5
Q
Large Vessel Thrombotic Stroke
Mechanisms
A
-
Atherosclerotic
- Large vessel atheroma with fibrous cap ruptures ⇒ plaque hemorrhage ⇒ exposes collagen and cholesterol to the lumen ⇒ promotes platelet aggregation and thrombosis
- Older patients
-
Dissection
- Occurs mostly in the carotid or vertebral arteries
- Abnormal elastin and collagen in media ⇒ allows blood to dissect ⇒ narrowing of lumen ⇒ slow sluggish flow ⇒ clot formation
- Consider in younger patients
- Risk factors: Marfan’s, Ehlers Danlos, hx of trauma
Can involve any of these vessels or their branches.
6
Q
Large Vessel Thrombotic Strokes
Subtypes
A
2 types of thrombotic stroke:
-
Thrombo-occlusive: clot occludes flow
- Clot completely occludes the diseased vessel then coagulated blood extends all the way up into the brain
- Generally, a large stroke in the distribution of that large vessel: carotid or vertebral
- Often preceded by TIA’s with very similar deficits each time that “crescendo” in severity and duration with each TIA
-
Thromboembolic: artery to artery embolism
- Near occlusion of the parent vessel results in clot formation over the atheroma or dissection
- Partial flow ⇒ clot enlargement ⇒ can break off and travel downstream where it lodges in a branch
- Ex: internal carotid → middle cerebral artery or vertebral artery → posterior cerebral artery
7
Q
Stroke Severity
A
- Size of the infarct also determined by adequacy of the collaterals
- Collateral flow ⇒ other vessels that also contribute flow to that region
- Older patients with diffuse atherosclerotic disease have poorer collaterals and bigger strokes
- Younger patients with the same clot may have milder deficits
8
Q
Carotid Artery Disease
Overview
A
- Carotid atheroma responsible for most anterior circulation large vessel thrombotic strokes
- Most disease is in the carotid bifurcation in the neck
- Mostly atherosclerotic in older and dissection in young
9
Q
Carotid Artery Disease
Symptomatic Stenosis
A
- Motor or sensory TIA or stroke appropriate to the ipsilateral carotid
-
Transient monocular blindness (amaurosis fugax) appropriate to the ipsilateral carotid
- Shade-like loss of vision
- Caused by arterial embolism from carotid → central retinal artery
10
Q
Carotid Artery Disease
Management
A
-
Treatment: aggressive medical management
- Treatment of lipids and HTN
- Antiplatelet therapy: aspirin, clopidogrel (Plavix), aspirin plus dipyridamole (Persantine) ⇒ nucleoside transport inhibitor and PDE3 inhibitor that inhibits blood clot formation
- If symptomatic and stenosis > 60% or an ulcerated plaque ⇒ can do endarterectomy or stent (NASCET criteria)
- Asymptomatic stenosis > 80% ⇒ endarterectomy or stent (ACAS criteria)
- Endarterectomy ⇒ remove the diseased lining and let the artery form a new endothelium
- Stent ⇒ inflate a balloon that leaves a metal mesh that compresses the atheroma and allows re-establishment of blood flow
11
Q
Vertebral Artery Disease
A
Vertebrobasilar disease accounts for 10% of posterior circulation large vessel thrombotic strokes.
- Atherosclerosis in the older patient or dissection in the young
- Also thrombotic
- Treated same as carotid with aggressive medical management and antithrombotic therapy
- Unlike the carotid, there are no invasive options such as endarterectomy (inaccessible) or stenting (dangerous and ineffective)
12
Q
Aortic Arch
Thromboembolic Stroke
A
- 10% of all thromboembolic strokes
- Seen best with transesophageal echo (TEE)
- Usually atherosclerotic
- Tx: maximal medical therapy like for carotid
- No stenting or surgery
13
Q
Intracranial Atherosclerosis
A
- Atherosclerosis of the brain arteries causes thrombotic strokes
- Presents with recurrent stereotypical TIAs with increasing deficits: crescendo TIA’s culminating in stroke
- Treatment is maximal medical therapy
- Rarely reopen artery with endovascular treatment: angioplasty or WINGSPAN-stent
14
Q
Intracranial Stenosis
Other Etiologies
A
-
Moya-moya
- Rare in US; seen more in Asia
- Vasculitis of the major cerebral arteries
- Collaterals open up and have appearance of puff of smoke on angiogram “moya moya” in Japanese
- Can be secondary to sickle cell
- Vasculitis, granulomatous arteritis, fibromuscular dysplasia ⇒ rare causes of intracranial stenosis
- Infectious arteritis: TB, CMV, syphilis, Herpes zoster in immunocompromised
15
Q
Lacunar Infarcts
A
- Small vessel thrombotic strokes and chronic white matter ischemia
- Each major cerebral vessel → superficial cortical branch & deep branches
- Small deep vessels supply the deep white matter including internal capsule, thalamus, basal ganglia and pons
- Small perforating vessels close off ⇒ thrombotic small vessel disease and occlusion
- When a single deep branch occludes ⇒ very small part of brain is infracted called a lacune (“little lake”) ⇒ limited deficits
16
Q
Lacunar Syndromes
A
-
The lacunar syndromes include:
- Pure sensory stroke (involves part of the thalamus)
- Clumsy hand dysarthria (involves part of the internal capsule)
- Ataxic hemiparesis
- When multiple and bilateral, esp. involving white matter corticobulbar tracts ⇒ pseudobulbar affect: inappropriate laughing and crying
17
Q
Lacunar Infarcts
Pathogenesis
A
-
Lipohyalinosis
- Progressive thickening of the intima and eventual closure of the lumen of the small perforating arteries ⇒ lacunar infarcts
- Major cause is HTN
- Lipohyalinosis can also cause the same vessels to rupture ⇒ ICH
- Some lacunes are due to atherosclerosis of the ostia of the small penetrating arteries
- More likely to involve multiple adjacent small arteries
- Larger lacunes ⇒ “lagoonar infarcts”
18
Q
Small Vessel Disease
Radiologic Changes
A
- Can cause white matter changes on MRI and CT called leukoaraiosis
- Common MRI reading is “evidence of white matter disease / subclinical ischemia”
-
When moderate, a normal finding in older patients especially with migraine and HTN history
- Causes unnecessary alarm to patients when they read these reports
- When extensive, can result in cognitive impairment or even vascular dementia
19
Q
Small Vessel Disease
Treatment
A
- Treat risk factors
- Esp. HTN, DM
- Antiplatelet therapy
20
Q
Cardio-embolic Strokes
Characteristics
A
-
Atrial fibrillation most common cause
- Accounts for ~ 15% of strokes in the US
- ↑ Frequency of A. Fib as more Americans survive to 9th decade
- Most clots form in the left atrial appendage ⇒ “left atrial cardiomyopathy”
-
Certain features suggest cardioembolic stroke:
- Sudden onset, can be large
- Wedge-shaped cortical infarcts
- Acute strokes involving anterior and posterior circulation or right and left hemispheres simultaneously
- Strokes in posterior circulation and cerebellum
- Stroke in language areas with aphasia
21
Q
Cryptogenic Stroke
A
A brain infarction not clearly attributable to a definite cardio-embolism, large artery atherosclerosis, or small artery disease despite extensive investigation.
Often from A. Fib.
22
Q
Atrial Fibrillation
Evaluation
A
- Prolonged cardiac monitoring: loop recorder
- 2D echo
- TEE
- Better imaging of LA appendage
- Certain patterns suggest embolic source in LAA
23
Q
Atrial Fibrillation Related Stroke
Treatment
A
-
Oral anticoagulation
- Warfarin had been the pharmacologic standard for stroke risk reduction in pts with A. Fib
- Novel oral anticoagulants ⇒ equally effective w/ fewer ICH ⇒ now tx of choice
- Dabigatran, rivaroxaban, apixaban, edoxaban
-
A. Fib w/o hx of stroke management ⇒ anticoagulation based on CHADS2vasc score
- Elderly w/ a gait disorder is not a contraindication for anticoagulation
- Need to fall 800 times to exceed risk of harm from single stroke
24
Q
Cardiogenic Strokes
Other Etiologies
A
- Acute MI with dyskinetic segment ⇒ mural thrombus
- Rheumatic heart disease and mechanical valve replacement
- SBE (subacute bacterial endocarditis) ⇒ vegetations ⇒ septic emboli to brain ⇒ infarct (often hemorrhagic)
- Left atrial myxoma ⇒ tumor fragments and travels distally
- SLE ⇒ Libman Sachs endocarditis
- Cancer: hypercoagulable state with marantic endocarditis and emboli
- Severe CHF
- Cardiac bypass pump during CABG
- Patent foramen ovale (PFO)
- Fat embolism ⇒ after long bone fracture
- Air embolism ⇒ accidentally infusing air into venous or arterial circulation or decompression sickness in diver
25
Q
Patent Foramen Ovale (PFO)
Related Stroke
A
- Consider in young person with no classic risk factors: HTN, DM, HLD
- Paradoxical embolism from venous clot across the PFO
- Often thrombophilia as well: factor V Leiden, prothrombin gene mutation 20210A, protein S, protein C, antithrombin-3
- Can be closed but controversial tx
26
Q
Watershed Infarcts
A
- Infarction caused by decreased blood flow
- Most distal vessels first to lose perfusion
- Combo of large vessel stenosis (carotid, vertebral), upstream stenosis, heart failure (low CO), and poor collaterals
- Post cardiac arrest: no flow to the brain for minutes, the watershed zones are infarcted first
- Locations:
-
Cortical border zone infarcts
- Between 2 vessels both with low flow
- ACA-MCA ⇒ trunk weakness
- MCA-PCA ⇒ if b/l prosopagnosia
- Between 2 vessels both with low flow
-
Internal border zone infarcts
- Between superficial and deep vessels off a major artery
- MCA-lenticulostriates
- PCA-thalamoperforators
- ACA-Huebner’s
- Between superficial and deep vessels off a major artery
-
Cortical border zone infarcts
- String of pearls on MRI
27
Q
Cortical Venous Infarcts
Overview
A
- Hemorrhagic infarcts due to partial or complete venous sinus or cortical vein thrombosis
- Not typical distribution of arterial infarcts ⇒ can be B/L or cross expected arterial boundaries
-
See unusual pattern of deficits:
- Saggital sinus thrombus ⇒ bilateral weakness
- More seizures
- Papilledema
- Headache
28
Q
Cortical Venous Infarcts
Pathophysiology
A
-
Combo of edema and ischemia:
- Blood cannot drain into sinus ⇒ back pressure into thin-walled veins ⇒ extravasation of RBCs along with infarction
- Hemorrhagic conversion common
- Especially irritating for the brain ⇒ more likely to induce seizures
29
Q
Venous Thrombosis
Risk Factors
A
- Post-partum
- Chemotherapy
- Underlying infection, inflammation, or malignancy
- Women on contraceptives
- Thrombophilia (ex. TPO)
- Neurosurgery ⇒ meningioma resection (damage the venous sinus)
30
Q
Cortical Venous Infarcts
Management
A
-
Diagnosis:
- MRI brain w/gadolinium and MR venography
- CT brain w/ contrast and CT venography
-
Treatment:
- Anticoagulation even though may be a hemorrhagic infarct as likely to progress
- Extreme cases of massive cortical venous sinus thrombosis: continuous tPA infusion into the sinus
- Look for underlying cause cancer
31
Q
Transient Ischemic Attack (TIA)
A
- A transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction ⇒ reversible cerebral ischemia
- Same underlying pathology as stroke but completely reverses
- Higher risk of a subsequent stroke and if occurs ⅓ will be in the next 48 hours
- Workup: MRI shows if infarct, image carotids, echo of heart, EKG monitoring for A. Fib
- Most are admitted
32
Q
Stroke Presentation
Overview
A
- Sx depends on which vessel closes
- Clinical presentation often suggests etiology:
- Sudden ⇒ embolic
- Stuttering ⇒ more thrombotic
33
Q
Brain
Functional Areas
A
34
Q
Middle Cerebral Artery (MCA)
Complete Occlusion
A
Anterior circulation stroke
-
Frontal and parietal lobes affected:
- Weakness and sensory loss, arm greater than leg
- If dominant hemisphere ⇒ aphasia
- If complete ⇒ life threatening
- Eyes “looking toward the lesion”
35
Q
Middle Cerebral Artery (MCA)
Branch Occlusions
A
Anterior circulation stroke
- Temporo-parietal: Wernicke’s receptive aphasia
- Frontal: Broca’s expressive aphasia
- Frontal motor strip: contralateral weakness
- Parietal sensory strip: contralateral sensory loss
- Nondominant parietal lobe: hemineglect
- Dominant parietal lobe: ideomotor apraxia
37
Q
Posterior Circulation Stroke
Overview
A
- Vertebral artery disease causes posterior circulation stokes
- Extracranial or intracranial vertebral, basilar and PCA occlusions
- See various brainstem stroke syndromes
38
Q
Brainstem
Nuclear Columns
A
-
Medial** **⇒** **motor
- Very medial: somatic motor ⇒ tongue and eye movements
- Medial: branchiomotor ⇒ facial, jaw, and swallowing and voice muscles
-
Lateral** **⇒** **sensory
- Lateral: trigeminal nucleus ⇒ ipsilateral facial sensation
- Far lateral: special sensory ⇒ vestibular nuclei (huge representation in medulla and pons), cochlear nucleus
39
Q
Brainstem
Pathways
A
Also medial ⇒ more motor & lateral ⇒ more sensory
-
Medial:
- Descending motor: corticospinal tract ⇒ contralateral body weakness (crosses at medullary pyramid)
- Corticobulbar ⇒ dysarthria
-
Medial/Lateral:
- Descending sympathetic motor tracts ⇒ pupil, eyelid, facial sweat ⇒ ipsilateral Horner’s syndrome
-
Lateral:
- Ascending sensory pain and temperature (STT) from contralateral body (crosses in cord) ⇒ contralateral anesthesia body
-
Far lateral:
- Cerebellar connections (peduncles)
40
Q
Wallenberg Syndrome
Etiology
A
-
Occlusion of the PICA (posterior inferior cerebellar artery)
- Final branch of the vertebral artery before it joins to form the basilar artery
- Can be seen with distal vertebral artery occlusion
- One of the most common brainstem strokes
- Often misdiagnosed as inner ear disturbance or gastroenteritis
41
Q
Wallenberg Syndrome
Clinical Manifestations
A
Classic brainstem infarct involving the lateral medulla
-
Medial part of lateral medulla ⇒ motor
- Nucleus ambiguus [motor nucleus of vagus] ⇒ palate and larynx → dysphagia and hoarseness
- Descending sympathetics ⇒ ipsilateral Horner’s syndrome (ptosis, miosis, anhidrosis)
-
Lateral part ⇒ sensory
- Descending nucleus/tract of trigeminal ⇒ ipsilateral loss of pain and temperature from face
- Spinothalamic tract ⇒ contralateral loss of pain and temperature from body
- Vestibular nuclei ⇒vertigo, N/V, nystagmus
- Far lateral:
- Inferior cerebellar peduncle ⇒ ipsilateral ataxia
42
Q
AICA Syndrome
A
Infarct affects lateral caudal pons
-
Similar to Wallenberg syndrome except:
- Also see tinnitus and hearing loss, facial weakness
- No motor weakness of swallowing and voice
43
Q
Paramedian Pontine Infarcts
A
- Lacunar infarcts from small vessel disease of the paramedian pontine perforators
- Clinically the same as lacunes higher up in internal capsule
- Motor deficits from corticospinal/ corticobulbar tracts ⇒ limited weakness, dysarthria
44
Q
Hemi-Pontine Infarct
A
Larger territory of unilateral pons infarcted ⇒ “lagoonar infarct”
- ↑ Corticospinal / corticobulbar tract involvement ⇒ ↑weakness and dysarthria
- If 6th CN nerve nucleus affected (abducens) ⇒ cannot move the eyes laterally so the eyes drift medially
- Look away from the lesion ⇒ “wrong way eyes”
- Vs MCA infarct ⇒ look at the lesion
- Look away from the lesion ⇒ “wrong way eyes”
- Atherosclerosis of basilar artery knocks off many perforators
- Ominous as could next occlude the whole basilar artery
45
Q
Basilar Artery Occlusion
A
Total basilar artery occlusion ⇒ total pons infarction
- Causes Locked In Syndrome
- Fully awake (reticular activating system spared - is in the midbrain)
- Quadriplegic except for vertical eye movements and blink
- Both 6th CN nuclei involved ⇒ no lateral eye movement
46
Q
Top of the Basilar
Syndrome
A
Usually embolic from the vertebral artery or heart
Infarct directly affects midline aspect of midbrain ⇒ Weber Syndrome
-
CN III nuclei ⇒ somatic and parasympathetic motor fibers ⇒ 3rd nerve palsy
- Ipsilateral lateral strabismus
- Ptosis
- Dilated pupil
- Ophthalmoplegia
- Loss of accommodation
- Loss of pupillary reflex
-
Long tract signs:
- Corticospinal tract ⇒ contralateral spastic hemiparesis
- Corticobulbar tract ⇒ contralateral lower face weakness, drooping of the corner of the mouth
-
Leads to clotting into bilateral PCA distributions
- Occipital lobe ⇒ homonomous hemianopsia (loss of the same half of vision in both eyes)
- Temporal lobe (hippocampus) ⇒ anterograde amnesia (cannot learn new info)
49
Q
Acute Ischemic Stroke
Management
A
- ± Admin of tPA
- Lower BP only to acceptable range for IV tPA tx: systolic < 185, diastolic < 110
- Consider thrombectomy and transfer to comprehensive stroke center ⇒ “drip and ship”
- Large clots that IV tPA cannot reach
- Hyperdense MCA sign on CT
- Does not exclude patient from tPA or thrombectomy
- Recent trials show that stent retrievers used early better long-term outcomes
- Admission to a stroke unit
- PT and begin regular exercise as tolerated
- Reintegration into community
50
Q
Tissue Plasminogen Activator (tPA)
Overview
A
“Clot buster” drug
- Given within 3-hour window of first signs of stroke
- Can give at 4.5 hours in select pts with some exclusions
- Careful selection to avoid hemorrhagic conversion: 2.7% risk
- 100 patients: 16 benefit, 2.7 harm, the rest no difference
-
Tx goals:
- Recanalize blocked artery
- Preserve the ischemic penumbra
54
Q
Primary Intracerebral Hemorrhage (ICH)
Definition
A
Bleeding in the brain parenchyma due to a ruptured vessel.
Deep vs lobar
55
Q
Secondary Intracerebral Bleed
Definition
A
Hemorrhagic conversion of a lesion as infarct or tumor.
56
Q
Intraventricular Bleed
Definition
A
Rupture of parenchymal bleed into the ventricles generally from hypertensive bleed.
57
Q
Subarachnoid Hemorrhage
Definition
A
Blood in the subarachnoid space generally from ruptured aneurysm or trauma.
58
Q
Subdural Hematoma
Definition
A
Blood in space between the dura and pia/arachnoid from trauma.
59
Q
Epidural Hematoma
Definition
A
Blood between the calvarium and the dura from trauma.
60
Q
Obstructive Hydrocephalus
Definition
A
Blockage of CSF flow due to blood in the ventricular system.
61
Q
Peri-Hematoma Edema
Definition
A
Area surrounding the bleed
62
Q
Intracerebral Hemorrhage (ICH)
Overview
A
- Common cause of disability and death
- Estimated annual incidence of 33 people per 100k
- 5% die before arrival at medical facilities
- For the majority that survive, overall prognosis is grave:
- 35% dying within 7 days
- 50% by 30 days
- Large bleeds have up to 80% mortality
- Expansion in first 1-3 days common ⇒ when clinical deterioration occurs
64
Q
Deep Hypertensive Parenchymal
Hemorrhages
A
- The most common and most lethal of bleeds
-
Due to small vessel disease
- Damage of endothelium by chronic HTN w/ resultant lipohyalinosis
- Same vessels and pathologic process of lacunes and same distribution
- Small perforating arteries to deep structures
- Basal ganglia, internal capsule, thalamus and pons
- Instead of the occlusion that causes lacunar infarcts, there is vessel rupture causing deep bleeds
66
Q
Deep Parenchymal ICH
Complications
A
- Cerebral herniation
-
Obstructive hydrocephalus when ventricular extension
- Drains often ineffective
- Clot off
- Blood in ventricle a poor prognostic sign
- Drains often ineffective
68
Q
Lobar Hematomas
Overview
A
- More superficial bleeds, somewhat better prognosis
- Most often due to cerebral amyloid angiopathy (CAA) or contusion
- DDx: AVM’s, aneurysm, hemorrhagic transformation of infarct/tumor
-
Often amenable to surgical removal if mass effect and incipient herniation
- Especially when in cerebellum ⇒ temporal lobe near surface and accessible
69
Q
Cerebral Amyloid Angiopathy
(CAA)
A
Widespread deposition of beta amyloid in the small caliber vessels of brain making them more likely to rupture.
-
Amyloid in vessel walls ⇒ ↑ fragility and liable to rupture
- More superficial vessels
- Older patients often have coexisting Alzheimer’s
- Same amyloid in vessels as in brain parenchyma ⇒ Amyloid neuritic plaques
- Alzheimer’s not an absolute contraindication for lifesaving superficial clot evacuation
-
Microbleeds
- Macro-bleeds often in site of prior microbleed
- Presence may increase risk of anticoagulation related bleeds
- Exact risk not known
72
Q
Hemorrhagic Conversion
Arterial Stroke
A
-
Often embolic and large infarct
- Ischemia of the vascular endothelium then re-establish flow
-
Can be post tPA
- More when protocol violations
- Supportive Tx, reversal???
- Prevention
- In large stroke from A. Fib, wait 1 week to begin anticoagulation
74
Q
Hemorrhagic Conversion of Tumors
A
-
Primary
- Glioblastoma multiforme (GBM)
- Very vascular and necrotic so often bleeds
-
Metastatic
- Especially melanoma, renal cell which are very vascular
- Treat w/ corticosteroids for vasogenic edema
75
Q
Cerebral Aneurysm Rupture
Overview
A
- Mostly in Circle of Willis
- Most rupture into peri-chiasmatic cistern ⇒ subarachnoid hemorrhage
- Rarely aneurysm rupture aims into the brain ⇒ parenchymal bleed
- Re-rupture common
- Day 3-5 vasospasm common
- Multiple strokes and high mortality
- Need early clipping or coiling of aneurysm (day 1-2) so hypervolemic/hypertensive therapy can be given without re-rupture before vasospasm sets in
- At first may not see aneurysm on angiogram because of arterial spasm
- Must repeat angiogram later
76
Q
Cerebral Aneurysm Rupture
Locations
A
3 most common locations to rupture:
Anterior Communicator (ACOM)
Middle Cerebral Artery (MCA)
Posterior Communicator (PCOM)
77
Q
Anterior Communicator (ACOM)
Rupture
A
- Most common to rupture (40%)
- Adjacent to optic chiasm and mesial basal frontal lobe so neighborhood signs of:
-
Visual field defects such as bitemporal heteronymous hemianopsia
- Due to compression of the optic chiasm
- Frontal lobe pathology
- Change in personality
-
Visual field defects such as bitemporal heteronymous hemianopsia
78
Q
Middle Cerebral Artery (MCA)
Rupture
A
- 2nd most common aneurysm to rupture (34%)
- Deep in temporal lobe
- Can present as a space occupying lesion causing temporal lobe seizures
- Can look like brain tumor and attempts at resection = disaster
79
Q
Posterior Communicator (PCOM)
Rupture
A
- 3rd most common site to rupture (20%)
- Runs over the exiting 3’d nerve so neighborhood signs of:
- Compressed 3’d nerve w/ blown pupil and ptosis and sparing eye movements
- “Surgical 3’d”
82
Q
Arteriovenous Malformations (AVM)
A
Direct connection of artery to vein without arterioles or capillaries intervening
- Arterial BP against thin-walled veins
- Result is tendency to catastrophic bleed
-
Extension of AVM to form many interconnected branches
- Difficult to tie off all of them
- Like “cutting the head off a medusa
- Cut one and 3 more pop-up”
- Treatment: Embolize first to close as many branches and feeder vessels prior to surgical excision
83
Q
Cavernous Hemangioma
(Cavernoma)
A
- Small malformed veins, low pressure and slow flow
-
Often leak but not life-threatening
- Causes local neurologic dysfunction that gradually clears
- E.g. brainstem location might cause dysarthria
- Causes local neurologic dysfunction that gradually clears
- Without imaging, can behave like ischemic stroke or multiple sclerosis plaque
- Often misdiagnosed as either
- No specific tx and prognosis favorable
- Can be multiple, often familial
84
Q
Cerebral Contusions
A
-
Coup lesions
- Direct force on brain at point of impact
-
Contrecoup
- Brain trauma on opposite side of head to direct trauma as result of brain moving through CSF and slamming into the calvarium
- Clues that it is traumatic: soft tissue swelling on exam and CT
- Frontal and temporal bones most common
- Increasing cause of cerebral bleeds w/ aging population and frequent falls
